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The comparison of stroke volume variation with central venous pressure in predicting fluid responsiveness in septic patients with acute circulatory failure.
Indian Journal of Critical Care Medicine 2015 July
PURPOSE: The present study was designed to investigate the efficacy of stroke volume variation (SVV) in predicting fluid responsiveness and compare it to traditional measures of volume status assessment like central venous pressure (CVP).
METHODS: Forty-five mechanically ventilated patients in sepsis with acute circulatory failure. Patients were not included when they had atrial fibrillation, other severe arrhythmias, permanent pacemaker, or needed mechanical cardiac support. Furthermore, excluded were patients with hypoxemia and a CVP >12. Patients received volume expansion in the form of 500 ml of 6% hydroxyethyl starch.
RESULTS: The volume expansion-induced increase in cardiac index (CI) was >15% in 29 patients (labeled responders) and <15% in 16 patients (labeled nonresponders). Before volume expansion, SVV was higher in responders than in nonresponders. Receiver operating characteristic curves analysis showed that SVV was a more accurate indicator of fluid responsiveness than CVP. Before volume expansion, an SVV value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 78% and a specificity of 89%. Volume expansion-induced changes in CI weakly and positively correlated with SVV before volume expansion. Volume expansion decreased SVV from 18.86 ± 4.35 to 7.57 ± 1.80 and volume expansion-induced changes in SVV moderately correlated with volume expansion-induced changes in CI.
CONCLUSIONS: When predicting fluid responsiveness in mechanically ventilated patients in septic shock, SVV is more effective than CVP. Nevertheless, the overall correlation of baseline SVV with increases in CI remains poor. Trends in SVV, as reflected by decreases with volume replacement, seem to correlate much better with increases in CI.
METHODS: Forty-five mechanically ventilated patients in sepsis with acute circulatory failure. Patients were not included when they had atrial fibrillation, other severe arrhythmias, permanent pacemaker, or needed mechanical cardiac support. Furthermore, excluded were patients with hypoxemia and a CVP >12. Patients received volume expansion in the form of 500 ml of 6% hydroxyethyl starch.
RESULTS: The volume expansion-induced increase in cardiac index (CI) was >15% in 29 patients (labeled responders) and <15% in 16 patients (labeled nonresponders). Before volume expansion, SVV was higher in responders than in nonresponders. Receiver operating characteristic curves analysis showed that SVV was a more accurate indicator of fluid responsiveness than CVP. Before volume expansion, an SVV value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 78% and a specificity of 89%. Volume expansion-induced changes in CI weakly and positively correlated with SVV before volume expansion. Volume expansion decreased SVV from 18.86 ± 4.35 to 7.57 ± 1.80 and volume expansion-induced changes in SVV moderately correlated with volume expansion-induced changes in CI.
CONCLUSIONS: When predicting fluid responsiveness in mechanically ventilated patients in septic shock, SVV is more effective than CVP. Nevertheless, the overall correlation of baseline SVV with increases in CI remains poor. Trends in SVV, as reflected by decreases with volume replacement, seem to correlate much better with increases in CI.
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